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Journal of Obstrectic Anaesthesia and Critical Care
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Year : 2014  |  Volume : 4  |  Issue : 1  |  Page : 50-52

Postpartum seizures with posterior reversible encephalopathy syndrome following cesarean delivery for triplets

Department of Anaesthesiology, Dr. D.Y. Patil Medical College, Hospital and Research Centre, Navi Mumbai, Maharashtra, India

Date of Web Publication20-May-2014

Correspondence Address:
Anita Chhabra
1603, 1604, Marathon Galaxy 1, LBS Road, Mulund (West), Mumbai - 400 080, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2249-4472.132830

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Posterior reversible encephalopathy syndrome (PRES) is a recently described clinicoradiologic entity that is associated with several medical conditions like hypertensive encephalopathy and eclampsia. It presents with rapid onset of symptoms including headache, seizures, altered consciousness, and visual disturbance. It is often, but not always associated with high blood pressure. We present a case of 23-year-old patient, with unremarkable antenatal period, who developed convulsions in the immediate postpartum period following elective cesarean delivery of her triplets performed under regional anesthesia. The magnetic resonance imaging brain revealed vasogenic edema suggestive of PRES. She was managed with supportive treatment including mechanical ventilation in the intensive care unit. She recovered completely without neurological sequelae and discharged on the 8 th postoperative day. This case report highlights the importance of awareness, prompt diagnosis and treatment to improve the outcome in this potentially life-threatening, but reversible condition.

Keywords: Cesarean delivery, eclampsia, posterior reversible encephalopathy syndrome, postpartum seizures, triplets

How to cite this article:
Chhabra A, Jagtap S. Postpartum seizures with posterior reversible encephalopathy syndrome following cesarean delivery for triplets. J Obstet Anaesth Crit Care 2014;4:50-2

How to cite this URL:
Chhabra A, Jagtap S. Postpartum seizures with posterior reversible encephalopathy syndrome following cesarean delivery for triplets. J Obstet Anaesth Crit Care [serial online] 2014 [cited 2023 Mar 27];4:50-2. Available from: https://www.joacc.com/text.asp?2014/4/1/50/132830

  Introduction Top

Seizures in the early postpartum period are a diagnostic dilemma. There may also be considerable overlap in presentation of the conditions making diagnosis and treatment difficult. Convulsions in the puerperium should be treated as eclampsia until proven otherwise. However, opportunities to identify other causes of convulsions should be vigorously pursued.

Posterior reversible encephalopathy syndrome (PRES) is a cliniconeuroradiologic entity described by Hinchey et al. in 1996. [1] It presents with neurologic signs and symptoms such as headache, altered consciousness, seizures, visual loss and often associated with abrupt increase in blood pressure (BP). It is associated with various medical conditions including hypertensive encephalopathy, eclampsia, renal failure, patients on immunosuppressant agents and cancer chemotherapy. [1] The unique neuroimaging findings of vasogenic edema are often symmetric, the parietal and occipital lobes being most commonly affected, followed by the frontal lobes, the inferior temporal-occipital junction and the cerebellum. [2] Various cases of PRES developed during peripartum period have been reported. [3] Here, we present a case of multiple pregnancy with uneventful antenatal course who developed PRES in the early postpartum period.

  Case report Top

A 23-year-old woman (gravida 2, para 1) was posted for elective cesarean section for safe confinement of triplets. Her antenatal period was uneventful with no prodromi of preeclampsia. Her routine blood and urine investigations done periodically were within normal range. Her BP ranged from 110/70 mm of Hg to 120/78 mm of Hg in the ante-natal period. A subarachnoid block with 2 ml of 0.5% bupivacaine was given at the L3-L4 space under aseptic precautions and once the sensory block up to T5 was achieved, the surgery was allowed and triplets were delivered. They had acceptable weight (1700, 1850, 2000 g) and good APGAR (8-9 at 1 min). There was an episode of unanticipated rise in BP to 160/100 mm of Hg with heart rate of 98/min, after the delivery of the triplets, with no accompanying relevant symptom or sign. To allay the patient's anxiety midazolam was administered after which the BP remained between 140/88 and 130/80 within the ensuing 10 min. The surgery lasted for 45 min and the blood loss was no more than 900 ml. The remaining intraoperative course was uneventful and patient was shifted to the recovery ward for observation. After 1΍ h, she complained of severe headache, followed by tonic-clonic convulsion and the BP recorded at that moment was high (160/100 mm of Hg). She was promptly treated with magnesium sulfate 4 g in 100 ml saline infused over 15 min and midazolam 1 mg intravenous (IV). In the postictal phase, her pulse rate was 114 beats/min, BP 150/90 mm of Hg and oxygen saturation of 100% with oxygen supplement. A neurological examination carried out after the convulsion episode was essentially normal without any sensory or motor deficit and fundoscopy was normal. Routine investigation showed hemoglobin of 11.3 g/dl, total leucocyte count of 17.3 × 10 3 /μL, platelets of 120 × 10 3 /μL, normal renal, and liver function tests and clotting parameters.

She was subsequently shifted to intensive care unit (ICU) for further management. In the ICU her treatment consisted labetalol, 10 mg IV slowly with continuous BP monitoring, Sodium phenytoin, 15 mg/kg IV loading dose followed by 100 mg IV TDS as maintenance and Magnesium Sulfate infusion, 1 g/h for control of BP and convulsion. After 18 h, in spite of being on medications, she had two more convulsions in quick successions following which she was promptly intubated using thiopentone 200 mg IV and Succinylcholine 50 mg IV and positive pressure ventilation was initiated with a volume control ventilator. An infusion of atracurium (5-10 mg/h) and midazolam (0.5-1 mg/h), titrated as per response, was also initiated to facilitate intermittent positive pressure ventilation. Her magnetic resonance imaging (MRI) on day two revealed bilateral hyperintensity on the T2-weighted and fluid-attenuated inversion recovery (FLAIR) sequences in the fronto-parietal, occipital cortical and subcortical white matter, bilateral corona radiata, cerebellar hemispheres and ganglio-thalamic regions with increased apparent diffusion coefficient values in these regions suggestive of vasogenic edema. These finding were consistent with PRES [Figure 1] and [Figure 2]. She was continued on the same supportive therapy of labetalol and sodium phenytoin and magnesium sulfate. She was closely monitored with all the necessary ICU protocols including periodic neurological assessment and biochemical profile. She was weaned off the ventilatory support successfully after 72 h following which she had an uneventful hospital stay and discharged on day 8 without any neurological sequelae.

A follow up MRI after 4 weeks showed complete resolution of the high signal foci and FLAIR signals previously noted.
Figure 1: Fluid-attenuated inversion recovery sequences showing bilateral hyperintense signal in the high frontal and parietal subcortical white matter

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Figure 2: T2 Fluid-attenuated inversion recovery sequences showing confluent hyperintensities in the subcortical white matter of occipital region

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  Discussion Top

Headache and seizure in the postpartum period without prodromi of pregnancy induced hypertension (PIH) in the antenatal period is a diagnostic dilemma. Eclampsia is the most likely cause unless proved otherwise. Multiple pregnancy does pose a greater risk to develop PIH in the mother. [4] The other probable causes could be cerebral venous sinus thrombosis, subarachnoid hemorrhage and postdural punctures seizures in the postpartum period. [5] In the present case the diagnosis of PRES was made following the typical radiological findings of bilateral, symmetrical cortical and subcortical vasogenic edema in combination with the characteristic presenting features. PRES is a cliniconeuroradiologic entity associated with varied medical conditions like hypertensive encephalopathy, PIH, eclampsia, renal failure, autoimmune disorders and patients on immunosuppressant medications and cancer chemotherapy. [1] Clinical findings include headache, visual changes, altered mental status, acute hypertension and seizures which are typically multiple. The key investigation for the diagnosis of PRES is cerebral MRI and not cerebral CT as the latter are often normal or nonspecific. [2] The typical MRI findings in T2-weighted and FLAIR sequences show hyperintense foci located bilaterally at the grey-white junctions, involving sub cortical white matter of most parts of brain; although it was earlier believed to affect the posterior parietal and occipital lobes mainly. [2],[6]

Global incidence of PRES is unknown. It has been reported in patients aged 4-90 years, although the most cases occur in age group of 39-47 years with a marked female predominance. [7] Mechanical ventilation is required in 35-40% of patients with PRES for 3-7 days. [8] Recurrence are reported to be occurring in 6% cases. Permanent neurologic damage is due to ischemia (10-23%) and hemorrhage (5-17%). Death is reported in 15% cases. [9]

The pathophysiology of PRES remains controversial suggesting two main hypotheses. Uncontrolled hypertension with failed autoregulation leads to hyperperfusion and cerebral vessel damage, resulting in interstitial extravasation of protein and fluid causing vasogenic edema, remains a popular consideration. The other theory alludes to systemic inflammatory state causing endothelial dysfunction leading to cerebral hypoperfusion which is then responsible for the disruption of the blood-brain barrier resulting in vasogenic edema. [10] Appropriate reduction of BP may prevent progression from vasogenic to cytotoxic edema resulting in cerebral infarction and permanent neurologic deficit. [11]

The association of PRES with toxemia of pregnancy is well-established. [12] PRES can occur, within several weeks after delivery and the clinical presentation is often confusing. [13]

Our patient who delivered three healthy triplets by an elective cesarean section was completely healthy and symptom-free during the antenatal period. No clinical trials have evaluated the management of PRES, but rapid withdrawal of the trigger appears to hasten recovery and avoid complications. For example, aggressive BP management, withdrawal of the offending drug, or delivery in eclampsia. Antiepileptic drugs should be used to treat seizures, and ventilatory support should be instituted in generalized status epilepticus and to protect the airway in obtunded patients. [14] In our patient, the seizure episode in the recovery room was managed effectively with magnesium sulfate. Mechanical ventilation [8] was helpful in preventing any cerebral hypoxia, hypercarbia and increased intra cranial pressure and as a consequence adverse neurological outcome. Prompt diagnosis and multidisciplinary management resulted in favorable outcome.

A clinical report of parturient with PRES after the delivery of triplets is presented. It emphasizes the need for early diagnosis and prompt treatment to avoid any short and long term neurological sequelae including death in a reversible condition like PRES.

  References Top

1.Hinchey J, Chaves C, Appignani B, Breen J, Pao L, Wang A, et al. A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996;334:494-500.  Back to cited text no. 1
2.Bartynski WS. Posterior reversible encephalopathy syndrome, part 1: Fundamental imaging and clinical features. AJNR Am J Neuroradiol 2008;29:1036-42.  Back to cited text no. 2
3.Long TR, Hein BD, Brown MJ, Rydberg CH, Wass CT. Posterior reversible encephalopathy syndrome during pregnancy: Seizures in a previously healthy parturient. J Clin Anesth 2007;19:145-8.  Back to cited text no. 3
4.Duckitt K, Harrington D. Risk factors for pre-eclampsia at antenatal booking: Systematic review of controlled studies. BMJ 2005;330:565.  Back to cited text no. 4
5.Shearer VE, Jhaveri HS, Cunningham FG. Puerperal seizures after post-dural puncture headache. Obstet Gynecol 1995;85:255-60.  Back to cited text no. 5
6.Casey SO, Sampaio RC, Michel E, Truwit CL. Posterior reversible encephalopathy syndrome: Utility of fluid-attenuated inversion recovery MR imaging in the detection of cortical and subcortical lesions. AJNR Am J Neuroradiol 2000;21:1199-206.  Back to cited text no. 6
7.Legriel S, Pico F, Azoulay E. Understanding posterior reversible encephalopathy syndrome. In: Vincet JL, editor. Annual Update in Intensive Care and Emergency Medicine. Vol. 1. Springer Berlin Heidelberg; 2011. p. 631-53.  Back to cited text no. 7
8.Burnett MM, Hess CP, Roberts JP, Bass NM, Douglas VC, Josephson SA. Presentation of reversible posterior leukoencephalopathy syndrome in patients on calcineurin inhibitors. Clin Neurol Neurosurg 2010;112:886-91.  Back to cited text no. 8
9.Lee VH, Wijdicks EF, Manno EM, Rabinstein AA. Clinical spectrum of reversible posterior leukoencephalopathy syndrome. Arch Neurol 2008;65:205-10.  Back to cited text no. 9
10.Bartynski WS. Posterior reversible encephalopathy syndrome, part 2: Controversies surrounding pathophysiology of vasogenic edema. AJNR Am J Neuroradiol 2008;29:1043-9.  Back to cited text no. 10
11.Wagner SJ, Acquah LA, Lindell EP, Craici IM, Wingo MT, Rose CH, et al. Posterior reversible encephalopathy syndrome and eclampsia: Pressing the case for more aggressive blood pressure control. Mayo Clin Proc 2011;86:851-6.  Back to cited text no. 11
12.Thackeray EM, Tielborg MC. Posterior reversible encephalopathy syndrome in a patient with severe preeclampsia. Anesth Analg 2007;105:184-6.  Back to cited text no. 12
13.Bartynski WS, Sanghvi A. Neuroimaging of delayed eclampsia. Report of 3 cases and review of the literature. J Comput Assist Tomogr 2003;27:699-713.  Back to cited text no. 13
14.Hobson EV, Craven I, Blank SC. Posterior reversible encephalopathy syndrome: A truly treatable neurologic illness. Perit Dial Int 2012;32:590-4.  Back to cited text no. 14


  [Figure 1], [Figure 2]

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